High-Glucose or -Fructose Diet Cause Changes of the Gut Microbiota and Metabolic Disorders in Mice without Body Weight Change.
High-Glucose or -Fructose Diet Cause Changes of the Gut Microbiota and Metabolic Disorders in Mice without Body Weight Change.
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DOI：
10.3390/nu10060761
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发表时间：
2018-06-13
期刊：
影响因子：
5.9
通讯作者：
Park HY
中科院分区：
文献类型：
--
作者：
Do MH;Lee E;Oh MJ;Kim Y;Park HY
高脂肪饮食诱导的肠道微生物群变化与肠道通透性和代谢性内毒素血症有关，后者与代谢紊乱有关。然而，高葡萄糖（HGD）或高果糖（HFrD）饮食对肠道微生物群的影响在很大程度上是未知的。我们通过16 S rRNA分析在HGD或HFrD喂养的C57 BL/6 J小鼠中进行肠道微生物群的变化。通过葡萄糖和胰岛素耐量试验、肠道通透性、Western blot和组织学分析评价肠道微生物源性内毒素诱导的代谢紊乱。我们发现HGD和HFrD组的血糖和内毒素水平、脂肪量、血脂异常和葡萄糖耐受不良相对较高，但体重没有变化。HGD和HFrD喂养的小鼠失去了肠道微生物多样性，其特征在于拟杆菌的比例较低，变形菌的比例显著增加。此外，HGD和HFrD组由于肠道炎症引起的紧密连接蛋白的改变而增加了肠道通透性。HGD和HFrD组的肝脏炎症和脂质蓄积也显著增加。饮食中高水平的葡萄糖或果糖调节肠道微生物群并增加肠道通透性，这在代谢性内毒素血症、炎症和脂质积累的发展之前，最终导致肝脂肪变性和正常体重肥胖。
High fat diet-induced changes in gut microbiota have been linked to intestinal permeability and metabolic endotoxemia, which is related to metabolic disorders. However, the influence of a high-glucose (HGD) or high-fructose (HFrD) diet on gut microbiota is largely unknown. We performed changes of gut microbiota in HGD- or HFrD-fed C57BL/6J mice by 16S rRNA analysis. Gut microbiota-derived endotoxin-induced metabolic disorders were evaluated by glucose and insulin tolerance test, gut permeability, Western blot and histological analysis. We found that the HGD and HFrD groups had comparatively higher blood glucose and endotoxin levels, fat mass, dyslipidemia, and glucose intolerance without changes in bodyweight. The HGD- and HFrD-fed mice lost gut microbial diversity, characterized by a lower proportion of Bacteroidetes and a markedly increased proportion of Proteobacteria. Moreover, the HGD and HFrD groups had increased gut permeability due to alterations to the tight junction proteins caused by gut inflammation. Hepatic inflammation and lipid accumulation were also markedly increased in the HGD and HFrD groups. High levels of glucose or fructose in the diet regulate the gut microbiota and increase intestinal permeability, which precedes the development of metabolic endotoxemia, inflammation, and lipid accumulation, ultimately leading to hepatic steatosis and normal-weight obesity.
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影响因子：
29
作者：
Jang C;Hui S;Lu W;Cowan AJ;Morscher RJ;Lee G;Liu W;Tesz GJ;Birnbaum MJ;Rabinowitz JD
通讯作者：
Rabinowitz JD
影响因子：
3.7
作者：
Lecomte V;Kaakoush NO;Maloney CA;Raipuria M;Huinao KD;Mitchell HM;Morris MJ
通讯作者：
Morris MJ
影响因子：
4.6
作者：
Han S;Jiao J;Zhang W;Xu J;Wan Z;Zhang W;Gao X;Qin L
通讯作者：
Qin L
影响因子：
4.5
作者：
Lim, Su-Min;Jeong, Jin-Ju;Kim, Dong-Hyun
通讯作者：
Kim, Dong-Hyun
影响因子：
3.2
作者：
Kim, Mee Kyoung;Han, Kyungdo;Park, Yong-Moon
通讯作者：
Park, Yong-Moon